Post transplant acute renal failure: a review.

Abstract

Post transplant acute tubular necrosis (ATN) is responsible for approximately 90% of acute renal failure episodes occurring within the first few weeks following renal transplantation. This phenomenon is observed in 34% of cadaver transplant recipients and 9% of those with live donor kidneys. Although the exact cause of post transplant ATN remains unknown, the following factors are thought to be associated with a higher incidence of ATN: 1) donor hypotension, 2) prolonged "warm ischemia time", 3) increased vascular resistance with poor perfusate flow, 4) presence of "ligandin" or excess lactate in the renal perfusate, 5) reduced allograft blood flow, 6) cold lymphocytotoxins in the patient's serum and 7) administration of nephrotoxic drugs particularly to the hypovolemic graft recipients. Therapeutic maneuvers such as hydration of the donors and recipients, harvesting the kidneys from heart beating cadavers, donor pretreatment with massive doses of corticosteroids and alpha-adrenergic blocking agents and warming of the graft immediately after vascular anastomosis, seem to reduce the incidence of ATN. Since the management differs significantly, post transplant ATN has to be distinguished from other causes of acute renal failure such as the renal artery thrombosis, hyperacute rejection and obstruction of the urinary tract. The tests which are of use in the differential diagnosis include, 131-I Hippuran renogram, transplant ultrasound, renal angiogram, retrograde pyelogram and renal transplant biopsy. Patients with established ATN should undergo every other day dialysis, under low dose or regional heparinization, until the creatinine clearance improves to 20 ml/min. The dose of azathioprine has to be reduced to prevent bone marrow toxicity. Even though there are short term disadvantages, the post transplant ATN does not appear to exert any detrimental effects in the long run. However, this issue remains controversial in the published reports.